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Blood, 1 May 2007, Vol. 109, No. 9, pp. 4020-4022. Prepublished online as a Blood First Edition Paper on January 3, 2007; DOI 10.1182/blood-2006-01-039586. This Article Full Text Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2006-01-039586v1 109/9/4020    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Morgado, E. Articles by Lavau, C. Search for Related Content PubMed PubMed Citation Articles by Morgado, E. Articles by Lavau, C. Related Collections Neoplasia Brief Reports Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief Report Flt3 is dispensable to the Hoxa9/Meis1 leukemogenic cooperation Ester Morgado1, Stéphanie Albouhair1, and Catherine Lavau1 1 Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche (UMR) 7151, Hôpital Saint-Louis, Paris, France HOX genes, MEIS1, and FLT3 are frequently up-regulated in human myeloid leukemias. Meis1 cooperates with Hox genes to induce leukemias in mice, hypothetically the consequence of Meis1-induced Flt3 overexpression. To test this, we compared the properties of Flt3–/– and Flt3+/+ progenitors transduced with Hoxa9 or Hoxa9/Meis1. In a myeloid clonogenic assay, Meis1 greatly enhanced the proliferation of Hoxa9-expressing cells, massively up-regulating Flt3 protein. However, the transforming potential of Hoxa9/Meis1 was unaltered in Flt3–/– cells. All mice that received Hoxa9/Meis1-transduced progenitors succumbed to rapid acute myeloid leukemias regardless of Flt3 genotype. Flt3 expression levels in leukemic blasts did not correlate with parameters reflecting their proliferative rate or their impaired differentiation. Furthermore, analysis of c-Myb expression levels in Hoxa9/Meis1-transformed cells showed that the up-regulation of this critical downstream effector was independent of Flt3. Altogether, our findings demonstrate that Flt3 is dispensable to the oncogenic cooperation of Meis1 with Hoxa9. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Survival signaling in HoxA9/Meis1 AML Gang G. Wang and Mark P. Kamps Blood 2007 109: 3619-3620. [Full Text] [PDF] This article has been cited by other articles: R. K. Slany The molecular biology of mixed lineage leukemia Haematologica, July 1, 2009; 94(7): 984 - 993. [Abstract] [Full Text] [PDF] B. Argiropoulos, E. Yung, and R. K. Humphries Unraveling the crucial roles of Meis1 in leukemogenesis and normal hematopoiesis Genes & Dev., November 15, 2007; 21(22): 2845 - 2849. [Full Text] [PDF]

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